Most blindness in the world today results fro abnormal (inadequate or excessive) immunoregulatory processes in the eye. Herpes Simples keratitis, for example, accounts for most corneal blindness in developed countries and most unilateral blindness in the United States. Prior to the detailed study of complex antigens such as those expressed or encoded by Herpes, it is necessary to determine basic featues of the immune response to more well-defined antigens or haptens. The intent of this study is to elucidate the genetic and cellular basis of immune reactions to the hapten azobenzenorsonate (ABA) coupled to cells and to study the molecular immunoregulation of these reactions in the eye. By using ABA cells, monoclonal suppressor factors we will determine the molecular bases of immune induction and regulation in the eye. By using ABA coupled to protein linked polyacrylamide beads we shall induce persistent inflammatory response in the anterior chamber and vitreous to develop a model of granulomatous 'uveitis.' Moreover, the cell constituents of acute and persistent inflammatory responses in the various chambers of the eye will be studied using fluoresceinated monoclonal reagents against T-cell subsets, B-cell subsets and macrophages. Finally, studies using anti I-J and I-A antibodies may help define therapeutic strategies to modulate a variety of ocular disease processes.